Evidence map›Paper›PMID 23092163›Full record

ArticleRetrovirology2012

SAMHD1: a new contributor to HIV-1 restriction in resting CD4+ T-cells.

Li Wu

Open access · goldAbstract read
In one paragraph

Article in Retrovirology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 30 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Li WuCenter for Retrovirus Research, Department of Veterinary Bioscience, The Ohio State University, 1900 Coffey Road, Columbus, OH 43210, USA. wu.840@osu.edu
The Ohio State University · US

Funding

The role of UBE2V1 in HIV-1 restriction in primary monocytesR21AI098524 · NIAID · OHIO STATE UNIVERSITY · PI WU, LI · 2012 to 2013
$419k
Novel host proteins in the HIV-1 preintegration complexesR21AI102822 · NIAID · OHIO STATE UNIVERSITY · PI WU, LI · 2012 to 2013
$406k
NIAID NIH HHS AI098524NIAID NIH HHS AI102822NIAID NIH HHS R21 AI098524NIAID NIH HHS R21 AI102822
6 · The paper itself

Abstract

Resting CD4+ T-cells are critical for establishing HIV-1 reservoirs. It has been known for over two decades that resting CD4+ T-cells are refractory to HIV-1 infection, but the underlying mechanisms are not fully understood. Compared with activated CD4+ T-cells that support HIV-1 infection, resting CD4+ T-cells have lower levels of dNTPs, which limit HIV-1 reverse transcription. The dNTPase SAMHD1 has been identified as an HIV-1 restriction factor in non-cycling myeloid cells. Two recent studies revealed that SAMHD1 restricts HIV-1 infection in resting CD4+ T-cells, suggesting a common mechanism of HIV-1 restriction in non-cycling cells that may contribute to viral immunopathogenesis.

Indexed as

CD4-Positive T-LymphocytesHIV-1HumansModels, BiologicalMonomeric GTP-Binding ProteinsNucleotidesReverse TranscriptionSAM Domain and HD Domain-Containing Protein 1Monomeric GTP-Binding ProteinsNucleotidesSAM Domain and HD Domain-Containing Protein 1SAMHD1 protein, human

Identifiers

PMID23092163
PMCPMC3492151
OpenAlexW2140810660

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.